ADENOSINE RELEASE FROM STIMULATED MAST-CELLS

ADENOSINE RELEASE FROM STIMULATED MAST-CELLS
复制标题

DOI:
10.1073/pnas.81.19.6192
复制
发表时间:
1984-01-01
期刊:
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA-BIOLOGICAL SCIENCES
影响因子:
--
通讯作者:
WASSERMAN, SI
WASSERMAN, SI
中科院分区:
其他
文献类型:
--
作者:
MARQUARDT, DL;GRUBER, HE;WASSERMAN, SI

文献摘要

被引文献

相似文献

暴露于缺氧条件或抗原攻击的肺组织中记录了腺苷释放。外源腺苷增强了受刺激的大鼠浆膜和小鼠骨髓来源的肥大细胞的介质释放。为了研究受刺激的肥大细胞产生和释放腺苷,在甲曲嗪梯度上纯化大鼠浆膜肥大细胞,并用抗二硝基苯酚IgE在37℃下敏化30分钟。 C并在1μM脱氧福霉素存在下用二硝基苯酚缀合的牛血清白蛋白抗原、Ca离子载体A23187或化合物48/80进行攻击。通过离心终止反应,并通过高效液相色谱法分别测定上清液和沉淀的腺苷和ATP含量。上清液的腺苷浓度从0.036±增加。用抗原、48/80 或 A23187 攻击 60 秒后,分别为 0.003 nmol/106 个细胞至 0.049、0.056 和 0.129 nmol/106 个细胞。离子载体刺激后,细胞外腺苷在 15 秒内明显增加,在 60 秒时达到峰值,并保持恒定至少 5 分钟。在 30 秒内观察到受刺激的 ATP 水平显着下降,这表明腺苷浓度的增加可能是由于 ATP 的分解造成的。在类似条件下培养的小鼠骨髓来源的肥大细胞也显示出 A23187 攻击后细胞外腺苷水平增加。这种内源性腺苷来源可能通过正反馈机制在局部发挥作用,以增强即时超敏反应。
Adenosine release was documented in lung tissue exposed to hypoxic conditions or antigen challenge. Exogenous adenosine potentiates mediator release from stimulated rat serosal and mouse bone marrow-derived mast cells. To investigate the production and release of adenosine from stimulated mast cells, rat serosal mast cells were purified on metrizamide gradients, sensitized with anti-dinitrophenol IgE for 30 min at 37.degree. C and challenged in the presence of 1 .mu.M deoxycoformycin with either dinitrophenol-conjugated bovine serum albumin antigen, the Ca ionophore A23187 or compound 48/80. Reactions were terminated by centrifugation, and the supernatants and pellets were assayed for adenosine and ATP content, respectively, by high performance liquid chromatography. The adenosine concentration of the supernatants increased from 0.036 .+-. 0.003 nmol/106 cells to 0.049, 0.056 and 0.129 nmol/106 cells 60 s after challenge with antigen, 48/80 or A23187, respectively. After ionophore stimulation, increased extracellular adenosine was evident by 15 s, peaked by 60 s, and remained constant for at least 5 min. A signficiant decline in stimulated ATP levels was observed within 30 s, suggesting that the enhanced adenosine concentrations may result from the breakdown of ATP. Cultured mouse bone marrow-derived mast cells under similar conditions also displayed augmented extracellular adenosine levels with A23187 challenge. This endogenous source of adenosine may act locally through a positive feedback mechanism to potentiate immediate hypersensitivity reactions.